Multiple sclerosis (MS) is a chronic inflammatory disease of the centr
al nervous system. T lymphocytes play a major role in the pathogenesis
of the disease. The exact mechanisms by which the inflammation is reg
ulated in MS have not yet been defined. Studies in animal models of MS
suggest that apoptosis of T cells is the main factor terminating infl
ammation. The process of apoptosis itself is regulated by a range of p
ro- and anti-apoptotic proteins. The bcl-2 gene family is an important
member of these proteins. The present study investigated the expressi
on of the anti-apoptotic protein bcl-2 in 11 chronic MS cases includin
g five relapsing-remitting and six chronic progressive MS patients. A
total of 35 lesions containing all stages of demyelinating activity we
re studied. The number of CD3-positive T cells and the absolute and re
lative numbers of T cells expressing bcl-2 were determined by double i
mmunocytochemistry. Bcl-2 is expressed by T lymphocytes in MS plaques.
Patients with chronic progressive MS have a higher proportion of bcl-
2 expressing T cells than patients with relapsing remitting disease. H
ighest numbers of bcl-2-positive T lymphocytes were found in remyelina
ting and demyelinated lesions, whereas active demyelinating lesions re
vealed lower numbers. These data indicate that cell-death-related prot
eins such as the anti-apoptotic protein bcl-2 are expressed in MS lesi
ons and that they might have important effects on the regulation of el
imination or persistence of inflammatory cells in the central nervous
system.